The Violinist's Thumb: And Other Lost Tales of Love, War, and Genius, as Written by Our Genetic Code (34 page)

Beyond the fact that you can spin DNA itself into art, the two intersect on more profound levels. The most miserable societies in human history still found time to carve and color and croon, which strongly implies that evolution wired these impulses into our genes. Even animals show artistic urges. If introduced to painting, chimpanzees often skip feedings to keep smearing canvases and sometimes throw tantrums if scientists take their brushes and palettes away. (Cross, sunburst, and circle motifs dominate their work, and chimps favor bold, Miró-esque lines.) Some monkeys also have musical biases as ruthless as any hipster’s,
^*
as do birds. And birds and other creatures are far more discriminating connoisseurs of dance than your average
Homo sapiens,
since many species dance to communicate or court lovers.

Still, it’s not clear how to fix such impulses in a molecule. Does “artistic DNA” produce musical RNA? Poetic proteins? What’s more, humans have developed art qualitatively different from animal art. For monkeys, an eye for strong lines and symmetry probably helps them craft better tools in the wild, nothing more. But humans infuse art with deeper, symbolic meanings. Those elks painted on cave walls aren’t just elks, they’re
elks we will hunt tomorrow
or
elk gods.
For this reason, many scientists suspect that symbolic art springs from language, since language teaches us to associate abstract symbols (like pictures and words) with real objects. And given that language has genetic roots, perhaps untangling the DNA of language skills can illuminate the origins of art.

Perhaps. As with art, many animals have hardwired protolanguage skills, with their warbles and screeches. And studies of
human twins show that around half of the variability in our normal, everyday aptitude with syntax, vocabulary, spelling, listening comprehension—pretty much everything—traces back to DNA. (Linguistic disorders show even stronger genetic correlation.) The problem is, attempts to link linguistic skills or deficits to DNA always run into thickets of genes. Dyslexia, for instance, links to at least six genes, each of which contributes unknown amounts. Even more confusing, similar genetic mutations can produce different effects in different people. So scientists find themselves in the same position as Thomas Hunt Morgan in the fruit fly room. They know that genes and regulatory DNA “for” language exist; but how exactly that DNA enhances our eloquence—increasing neuron counts? sheathing brain cells more efficiently? fiddling with neurotransmitter levels?—no one knows.

Given this disarray, it’s easy to understand the excitement, even hype, that attended the recent discovery of a purported master gene for language. In 1990 linguists inferred the gene’s existence after studying three generations of a London family known only (for privacy) as the KEs. In a simple pattern of single-gene dominance, half the KEs suffer from a strange suite of language malfunctions. They have trouble coordinating their lips, jaws, and tongues, and stumble over most words, becoming especially incomprehensible on the phone. They also struggle when asked to ape a sequence of simple facial expressions, like opening their mouths, sticking out their tongues, and uttering an
uuuuaaaahh
sound. But some scientists argue that the KEs’ problems extend beyond motor skills to grammar. Most of them know the plural of
book
is
books,
but seemingly because they’ve memorized that fact. Give them made-up words like
zoop
or
wug,
and they cannot figure out the plural; they see no connection between
book
/
books
and
zoop
/
zoops,
even after years of language therapy. They also fail fill-in-the-blank tests about the past
tense, using words like “bringed.” The IQs of affected KEs sink pretty low—86 on average, versus 104 for nonaffected KEs. But the language hiccups probably aren’t a simple cognitive deficit: a few afflicted KEs have nonverbal IQ scores above average, and they can spot logical fallacies in arguments when tested. Plus, some scientists found that they understand reflexives just fine (e.g., “he washed him” versus “he washed himself”), as well as passive versus active voice and possessives.

It baffled scientists that one gene could cause such disparate symptoms, so in 1996 they set out to find and decode it. They narrowed its locus down to fifty genes on chromosome seven and were tediously working through each one when they caught a break. Another victim turned up, CS, from an unrelated family. The boy presented with the same mental and mandibular problems, and doctors spotted a translocation in his genes: a Philadelphia-like swap between the arms of two chromosomes, which interrupted the
foxp2
gene on chromosome seven.

Like vitamin A, the protein produced by
foxp2
clamps onto other genes and switches them on. Also like vitamin A,
foxp2
has a long reach, interacting with hundreds of genes and steering fetal development in the jaw, gut, lungs, heart, and especially the brain. All mammals have
foxp2,
and despite billions of years of collective evolution, all versions look pretty much the same; humans have accumulated just three amino acid differences compared to mice. (This gene looks strikingly similar in songbirds as well, and is especially active when they’re learning new songs.) Intriguingly, humans picked up two of our amino-acid changes after splitting from chimps, and these changes allow
foxp2
to interact with many new genes. Even more intriguingly, when scientists created mutant mice with the human
foxp2,
the mice had different neuron architecture in a brain region that (in us) processes language, and they conversed with fellow mice in lower-pitched, baritone squeaks.

Conversely, in the affected KEs’ brains, the regions that help produce language are stunted and have low densities of neurons. Scientists have traced these deficits back to a single A-for-G mutation. This substitution altered just one of
foxp2
’s 715 amino acids, but it’s enough to prevent the protein from binding to DNA. Unfortunately, this mutation occurs in a different part of the gene than the human-chimp mutations, so it can’t explain much about the evolution and original acquisition of language. And regardless, scientists still face a cause-and-effect tangle with the KEs: did the neurological deficits cause their facial clumsiness, or did their facial clumsiness lead to brain atrophy by discouraging them from practicing language?
Foxp2
can’t be the only language gene anyway, since even the most afflicted in the KE clan aren’t devoid of language; they’re orders of magnitude more eloquent than any simian. (And sometimes they seemed more creative than the scientists testing them. When presented with the puzzler “Every day he walks eight miles. Yesterday he_____,” instead of answering, “
walked
eight miles,” one afflicted KE muttered, “had a rest.”) Overall, then, while
foxp2
reveals something about the genetic basis of language and symbolic thought, the gene has proved frustratingly inarticulate so far.

Even the one thing scientists had all agreed on with
foxp2—
its unique form in humans—proved wrong.
Homo sapiens
split from other
Homo
species hundreds of thousands of years ago, but paleogeneticists recently discovered the human version of
foxp2
in Neanderthals. This might mean nothing. But it might mean that Neanderthals also had the fine motor skills for language, or the cognitive wherewithal. Perhaps both: finer motor skills might have allowed them to use language more, and when they used it more, maybe they found they had more to say.

All that’s certain is that the
foxp2
discovery makes another debate about Neanderthals, over Neanderthal art, more urgent. In caves occupied by Neanderthals, archaeologists have discovered
flutes made from bear femurs, as well as oyster shells stained red and yellow and perforated for stringing on necklaces. But good luck figuring out what these trinkets meant to Neanderthals. Again, perhaps Neanderthals just aped humans and attached no symbolic meaning to their toys. Or perhaps humans, who often colonized Neanderthal sites after Neanderthals died, simply tossed their worn-out flutes and shells in with Neanderthal rubbish, scrambling the chronology. The truth is, no one has any idea how articulate or artsy-fartsy Neanderthals were.

So until scientists catch another break—find another KE family with different DNA flaws, or root out more unexpected genes in Neanderthals—the genetic origins of language and symbolic art will remain murky. In the meantime we’ll have to content ourselves with tracing how DNA can augment, or make a mess of, the work of modern artists.

No different than with athletes, tiny bits of DNA can determine whether budding musicians fulfill their talents and ambitions. A few studies have found that one key musical trait, perfect pitch, gets inherited with the same dominant pattern as the KE language deficit, since people with perfect pitch passed it to half their children. Other studies found smaller and subtler genetic contributions for perfect pitch instead, and found that this DNA must act in concert with environmental cues (like music lessons) to bestow the gift. Beyond the ear, physical attributes can enhance or doom a musician as well. Sergei Rachmaninoff’s gigantic hands—probably the result of Marfan syndrome, a genetic disorder—could span twelve inches, an octave and a half on the piano, which allowed him to compose and play music that would tear the ligaments of lesser-endowed pianists. On the other mitt, Robert Schumann’s career as a concert pianist collapsed because of focal dystonia—a loss of muscle that caused
his right middle finger to curl or jerk involuntarily. Many people with this condition have a genetic susceptibility, and Schumann compensated by writing at least one piece that avoided that finger entirely. But he never let up on his grinding practice schedule, and a jerry-built mechanical rack he designed to stretch the finger may have exacerbated his symptoms.

Still, in the long, gloried history of ailing and invalid musicians, no DNA proved a more ambivalent friend and ambiguous foe than the DNA of nineteenth-century musician Niccolò Paganini, the violin virtuoso’s violin virtuoso. The opera composer (and noted epicurean) Gioacchino Rossini didn’t like acknowledging that he ever wept, but one of the three times he owned up to crying
^*
was when he heard Paganini perform. Rossini bawled then, and he wasn’t the only one bewitched by the ungainly Italian. Paganini wore his dark hair long and performed his concerts in black frock coats with black trousers, leaving his pale, sweaty face hovering spectrally onstage. He also cocked his hips at bizarre angles while performing, and sometimes crossed his elbows at impossible angles in a rush of furious bowing. Some connoisseurs found his concerts histrionic, and accused him of fraying his violin strings before shows so they’d snap dramatically midperformance. But no one ever denied his showmanship: Pope Leo XII named him a Knight of the Golden Spur, and royal mints struck coins with his likeness. Many critics hailed him as the greatest violinist ever, and he has proved almost a singular exception to the rule in classical music that only composers gain immortality.

Paganini rarely if ever played the old masters during his concerts, preferring his own compositions, which highlighted his finger-blurring dexterity. (Ever a crowd-pleaser, he also included lowbrow passages where he mimicked donkeys and roosters on his violin.) Since his teenage years, in the 1790s, Paganini had labored over his music; but he also understood human psychology
and so encouraged various legends about the supernatural origins of his gifts. Word got around that an angel had appeared at Paganini’s birth and pronounced that no man would ever play the violin so sweetly. Six years later, divine favor seemingly resurrected him from a Lazarus-like doom. After he fell into a cataleptic coma, his parents gave him up for dead—they wrapped him in a burial shroud and everything—when, suddenly, something made him twitch beneath the cloth, saving him by a whisker from premature burial. Despite these miracles, people more often attributed Paganini’s talents to necromancy, insisting he’d signed a pact with Satan and exchanged his immortal soul for shameless musical talent. (Paganini fanned these rumors by holding concerts in cemeteries at twilight and giving his compositions names like “Devil’s Laughter” and “Witches’ Dance,” as if he had firsthand experience.) Others argued that he’d acquired his skills in dungeons, where he’d supposedly been incarcerated for eight years for stabbing a friend and had nothing better to do than practice violin. More sober types scoffed at these stories of witchcraft and iniquity. They patiently explained that Paganini had hired a crooked surgeon to snip the motion-limiting ligaments in his hands. Simple as that.

However ludicrous, that last explanation hits closest to the mark. Because beyond Paganini’s passion, charisma, and capacity for hard work, he did have unusually supple hands. He could unfurl and stretch his fingers impossibly far, his skin seemingly about to rip apart. His finger joints themselves were also freakishly flexible: he could wrench his thumb across the back of his hand to touch his pinky (try this), and he could wriggle his midfinger joints
laterally,
like tiny metronomes. As a result, Paganini could dash off intricate riffs and arpeggios that other violinists didn’t dare, hitting many more high and low notes in swift succession—up to a thousand notes per minute, some claim. He could double- or triple-stop (play multiple notes at
once) with ease, and he perfected unusual techniques, like left-handed pizzicato, a plucking technique, that took advantage of his plasticity. Normally the right hand (the bow hand) does pizzicato, forcing the violinist to chose between bowing or plucking during each passage. With left-handed pizzicato, Paganini didn’t have to choose. His nimble fingers could bow one note and pluck the next, as if two violins were playing at once.